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Path Exam II > Parasites pt 2 Toxoplasmosis - Leishmaniasis > Flashcards

Parasites pt 2 Toxoplasmosis - Leishmaniasis Flashcards

1
Q

Toxoplasma gondii: transmission

A

ingestion of oocysts in raw pork
inhalation of oocysts

inhalation of oocysts from cat feces

congenital: if a pregnant women is exposed to taxoplasma for the very first time, because she hasnt produced antibodies. she can pass to fetus. TORCHS

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2
Q

Toxoplasma gondii: morphology

A

oocysts is infectious

trophozoites

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3
Q

toxoplasma gondii: clinical findings

A

congenitally aquired (Torches)

results in still birth or live birth with symptoms early or later.

immunocompromised patietns disseminated infection with may include: encephalitis presenting as a brain mass. chorioetinitis. hepatosplenomegaly+lymphadenopathy
pneumonia

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4
Q

outcomes for child acquiring Toxoplasmosis transplacentally

A

chorioretinitis, blindness, seizures, mental retardation, microcephaly.

normal children may develop reactivation in adolescents– can lead to blindness.

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5
Q

Dignosis of Toxoplasmosis gondii

A

serology: high IgM and IgG
radiology: CT scan showing contrast enhancing mass in the brain
examination of the retina revealing retinal inflammation

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6
Q

what kind of microbe of T. gondii?

A

obligate intracellular parasites

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7
Q

Pneumocystis carinii: transmission

A

acquired early age via respiratory route. remains latent in normal host.

85% of children have had exposure asymptomatically. lives comfortably in people with intact immune systems. in AIDS and immunocompromised patients, it can multiply in the lungs and cause severe interstitial pneumonia

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8
Q

Penumocystis carinii: morphology

A

flying saucer appearing fungus in alveolar lung secretions (sputum samples)

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9
Q

pneumocystitis carinii: clinical findings

A

PCP interstitital pneumonia: fever, dry/unproductive cough. Most common opportunistic infection in patients with AIDS. 15% change of infection/year in AIDs patients. 80% lifetime risk without prophylactic therapy.

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10
Q

Pneumocystitis carinii: diagnosis

A

silver staining
flying saucer appearing fungi in saline induced sputum
brconhoalveolar lavage with bronchoscope. bronchial wall biopsy with bronchoscope. X-ray: find an interstitial pneumonia with diffuse infiltrates.

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11
Q

when are aids patients susceptible to pneumocystis carinii?

A

when their CD4 count is less than 200.

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12
Q

Plasmodium falciparum: episodes of chills and fevers

A

continuous

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13
Q

Plasmodium falciparum: continual reproduction in the liver?

A

no

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14
Q

Plasmodium falciparum: anemia?

A

yes

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15
Q

Plasmodium falciparum: sever clinical manifestations?

A

yes: brain and kidney

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16
Q

Plasmodium falciparum: chloroquine sensitivity?

A

no except in central america

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17
Q

Plasmodium vivax and ovale: episodes of fever and chills?

A

at 48 hr intervals

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18
Q

Plasmodium vivax and ovale: continual reproduction in the liver?

A

yes!!!!!!!

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19
Q

Plasmodium vivax and ovale: anemia?

A

yes

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20
Q

Plasmodium vivax and ovale: severe clinical manifestations

A

no

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21
Q

Plasmodium Malariae: fever and chills?

A

every 72 hrs

22
Q

Plasmodium Malariae: continual reproduction in the liver?

A

no

23
Q

Plasmodium Malariae: anemia?

A

yes

24
Q

Plasmodium Malariae: severe clinical manifestations?

A

no

25
Q

Plasmodium knowlesi: chills and fever?

A

not know

26
Q

Plasmodium knowlesi: continual reproduction in the liver?

A

no

27
Q

Plasmodium knowlesi: anemia?

A

yes

28
Q

Plasmodium knowlesi: severe clinical manifestations

A

yes

29
Q

plasmodium: transmission

A

anopheles mosquito

30
Q

plasmodium: morphology

A

several forms in life cycle. “hypnozoite stage” dormain form that hangs out in the liver

31
Q

plasmodium: clinical findings: vivax and ovale

A

every 48 hrs –> chills/fevers “tertian malaria”

hepatosplenomegaly caused by “duffy a” and “b” antigens

32
Q

plasmodium: clinical finding: Malariae

A

Quartan malaria: sweating/chills/fever every 72 hrs.

33
Q

Diagnosis of Plasmodium

A

blood smears: trophozoites “diamind ring shape”

34
Q

Babesia Microti: transmission

A

ixodes scapularis, the tick

35
Q

babesia microti: morphology

A

sporozoites from tick cause infection

sporozoites mature into trophozoites in humans and infect the RBCs

36
Q

babesia microti: clinical findings

A

immunocompetent ppl: asymptomatic

immunocompromised ppl: anemia due to hemolysis, fatigue, and protracted course

37
Q

babesia microti: diagnosis

A

blood smear, PCR, serology

“classic maltese cross” on blood smear. patients may be co infected with lyme disease

38
Q

Leishmania: mode of tranmission

A

sandfly bite, contaminated blood transfusion, zoonotic: carried by rodents, dogs, foxes.

39
Q

LEishmania: morphology

A

Promastigote: flagellated (inside the sandfly).
Amastigote: instracellular and nonflagellated (inside phagocytic cells of reticuloendothelial systems.

40
Q

Leishmania: clinical findings

A

cutaneous leishmaniasis- single ulcer at site of sandfly bite (oriental sore).

diffuse cutaneous: nodules at bite site (which do not ulcerate, especially near nose. can last up to 20 yrs without treatment

mucocutaneous: ulcers appear on mucous membranes after first ulcer at bite site heals. ulcers erode the nasal septum, soft palate, and lips. can last 20-40 ys.
visceral: leishmaniasis (kala-azar): comon in young, malnourished children. fever, anorexia, weight loss, and abdominal swelling from hepatomegalgy and massive splenomegaly. often fatal.

41
Q

which Leishmania has massive splenomegaly?

A

L. Donovani

42
Q

In whom will diffuse cutaneous leighmaniasis occur?

A

ppl with immunocompromised situations, malnurished ppl etc

because they dont have cell mediated immune response, L. skin test is negative

43
Q

how is a diagnosis of leishmaniasis made with those exhibiting mucocutaneous and cutaneous lesions?

A

mucocutaneous: skin scrapings
cutaneous: Leishmania skin test. cell mediated immunity

44
Q

Trypanosoma rhodesiense/gambiense: tranmission

A

TseTse fly. Following bite, flagellated form of these two organisms called Tryptomastigote spread via persons bloodstrewam to LNs and CNS

45
Q

Trypanosoma R/G: clinical manifestations

A

red painful skin ulcer that heals within 2 weeks. Systemic spread–> fever, headaches, dizziness and LN swelling. –> fever abates –> fever resumes –> fever abates .

CNS symptoms develop, drowsiness in the daytime, sleeping sickness) behavior changes, difficulty with walking, slurred speech, finally coma and death.

46
Q

what’s the big “pattern” in African sleeping sickness?

A

intermittent fevers followed by CNS problems, sleepiness, ataxia, slurred speech, coma and death.

47
Q

T. Brucei Gambiense is also called

A

West African Sleeping sickness

notable for slowly proressing fevers, wasting, late neuro symptoms.

48
Q

T. brucei rhodesiense is also called

A

East African Sleeping sickness. similar to west african variety but more severe. death occurs within weeks to months. rapid progression from recurrent fevers to early neurologic disease

49
Q

Amastigotes

A

rounded cells without flagella (both trypanosoma and leishmania)

50
Q

promastigotes, epimastiogtes, tryppmastigotes

A

flagellated motile forms (both trypanosoma and leishmania)

Path Exam II (7 decks)

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